Dr.S.Venkatesan MD

I am sure, this RCA shoot will stretch our coronary acumen

Video source and courtesy: Leizhi Ku,, Xiaojing Ma, From the Departments of Radiology (L.K.) and Echocardiography (X.M.), Wuhan Asia Heart Hospital, Wuhan, China

Did you guess the diagnosis correctly?

It is an acceptable diagnosis, if you thought an anomalous LCA, a LAD CTO or a single coronary artery. But, the true diagnosis is different. It is left main atresia .(Which can also be called a single coronary artery, if RCA gives origin to LCA)

How common are coronary artery anomalies?

It is about 1 to 2%. It can be in the origin, course, and termination. The common ones are the wrong sinus origin. Right arising from the left sinus is much more commoner than left arising from the right. This topic of anomalous origin needs a separate discussion. (Prachi P. Agarwal ,et al Radiographics 2017 )

Left main Atresia: Is it a sub-set of the anomalous origin of LCA from the right sinus ?

Technically yes, since the left coronary ostium is absent in its designated place in both conditions. But, the entity of true Left main atresia is rare and distinctly different.The difference is, that anomalous LCA often doesn’t travel in the pre-designated path of true LAD and LCX (Ie Intraventricular and Left AV groove). In true atresia, only the origin is sealed. Rest of the LCA is anatomically intact , which gets filled from one of three familiar Inter arterial collateral (Vieussens, Kugel, and retro-conal coronary ring)

Embryological basis of coronary artery anomalies

The left coronary anlagen and bud fail to develop. To know, how and why this happens ( Read here : Sharma B, Chang A, Red-Horse K. Coronary Artery Development: Progenitor Cells and Differentiation Pathways. Annu Rev Physiol. 2017 )

Clinical implication of such coronary anomalies

Apart from angiographic surprises, these anomalous coronary arteries may under-perfuse the ventricle and present as unexplained cardiomyopathy , until we realize the anatomical errors in coronary anatomy.

Some unanswered queries

1. Is the atresia confined to the ostium alone, or does it extend to variable lengths of the left main?

2. How do the fetal and subsequent neonatal LV mass outgrow RV , when the LCA is atretic?

Treatment of left main atresia

Surgery with graft makes logical correction. If absolutely asymptomatic, and the stress test is negative, leaving it, as it is, is not a forbidden option, in spite of the fact, that the patient would have a single coronary arterial supply.

Farhood Saremi Graydon Goodman , Alison Wilcox, J Am Coll Cardiol Img. 2011 Dec, 4 (12) 1320–1323

Acquired mimickers of left main atresia

1. Syphilis

2. Aorto arteritis

3.Ostial Athero-sclerosis( Rare, but status of other areas of coronary artery will usually reveal evidence for atherosclerosis)

True confirmation, is possible only during surgery , ie visulaing the absence of left coronary ostia.

Final message

Coronary arterial anomaly is a less discussed topic nowadays, unless & until, it intrudes an interventional cardiologist in his daily routine life, of delivering stents. In reality, there could be thousands of asymptomatic ones in the public domain. it can result in both risky as well as protective events. One theoretical and realistic possibility can be extrapolated. We know, how adverse is the outcome of Left main STEMI. But, It might also be true in a few lucky souls, one of the above rings can open up instantly and change the destiny.

Reference

1. Yassin AS, Dayco J, Kottam A. Left Main Coronary Artery Atresia: Diagnostic
   Images of a Rare Coronary Anomaly. Mayo Clin Proc 2023;98(5):655–656.
2. Musiani A, Cernigliaro C, Sansa M, Maselli D, De Gasperis C. Left main
   coronary artery atresia: literature review and therapeutical considerations.
   Eur J Cardiothorac Surg 1997;11(3):505–514.

June 2020

Let me go back … 4 years in time-line, to the dark COVID duty days in 2020 at one of the largest COVID facilities, Madras Medical College, Chennai.India.I still feel a sense of unease when I reflect on those harsh days, with bed-less patients gasping for breath and waiting in the long ambulance queues in our esteemed hospital.

I can’t recall how many times I was disrupted by the silent, final journey of body bags being transported to the mortuary ward. The fatigue and sickness affected doctors, fellows, nurses, and ward boys. Still, the hospital did a mind-boggling job of saving and caring for hundreds and thousands of patients through the agile administrative team.

June 2024

Putting those tough years back, I have since retired from my hospital. Now, why should I stumble upon this video from Dr Campbell. It shook me again. This is not an all-pervasive, fake, or exaggerated video clip from YouTube. It is, in my opinion, an uncontaminated truth. It took a 5-year chase to catch the truth, red-handed.

Dr John Campell don’t need any Introduction. He was the only comforting voice and his daily briefing right through the pandemic was watched by millions. Now, in June 2024, he has to say this. Watch it fully if you can. You will learn in 15 minutes, the lifetime lessons of how biomolecular & viral laboratories work. Also, be aware of the dangerous game of making gene sequences of these microbial monsters proprietary.

Also, don’t miss the thundering statement, by the ex CDC director, that has a huge implications for humanity, (Who himself is a virologist) The summary of the video seems to convey a strong message. Let us pray for no more pandemics. If at all it happens, let it be a natural one that will definitely be less virulent for sure.

Final message

The title of this post is intentionally provocative, However, there is no evidence to disprove it. One thing is clear. Hundreds of virulent viral RNA and DNAs are waiting in unknown labs, at various stages of mutations and gain in function, itching to get into an animal or human domain.

What a pity, “My dear world” I thought, our esteemed scientists are working day and night to weaken the viruses but they are using all their energy, and do just the opposite.

It looks like, the world is no longer a safe place to live in. We are adding more things to worry about than, War, Poverty & climate change. The solution is never going to come from the Governments or WHO. It is in our minds, in the ability to resist fear-mongering. Let the Almighty give us the capacity, to identify and avoid the evil design, that has encircled us, with deceiving kindness, topped up with sweetly poisoned science. (How can we forget those nearly 100 billion Dollars worth of senseless RTPCRs, CT scans Remdesvirs, and their clones, that went down the drain without any purpose.)

Further watching

More sinister truths are hidden in the widely open corridors of WHO headquarters.(Watch this video link)

Like coronary blood flow, intra-cardiac electricity must flow in a pre-designated path at a specific time interval with absolute  discipline. Any deviation or trespassing results in arrhythmia. While, minor aberrations are accepted, major deviations due to structural or functional reentry within the ventricles presenting as VTs (Scars, Infiltrates, etc) need immediate or at least early attention.

The term, VT mapping has been in vogue in clinical electrophysiology for more than half a century, right from Dr.Josephson and Wellens’ days. While , treating VTs with drugs is still a choice, permanent solutions by defining the VT circuit and ablating them, is the new norm. However , the difficulty is, demarcation of the VT circuit is still a tough job, especially since the VT circuit plays a mysterious hide-and-seek game during diastole. The current challenge is to draw the complete blueprint of the VT, especially the diastolic VT circuit.

The tracts that carry the diastolic electrical flow are located sub-endocardially, sub-epicardially , over right ventricular aspect, or finally through the ubiquitous concealed intramural paths.

Unless, we eliminate the entire circumference of the circuit the chances of recurrence is higher (This is contrary to the past belief that a one-time interruption of the VT circuit at some point of the circumference was considered good enough. (This is what DC shocks do for temporary reversion to sinus rhythm )

How to localize the diastolic pathways?

We must thank the technological innovators in the electro-anatomical mapping system, who are continuously upgrading and providing the best to us. The following image and video clip is one such demonstration of ablating hidden diastolic paths between the entry and exit points.

Diastolic blind spots between the entry & exit points of VT can be deep & dark

Next question in the queue

Can a VT occur without an exit point ? (I have been looking for a long time for an answer)

“Half-baked knowledge is not better than fully-baked Ignorance“

LDL is portrayed as villain de-chief of Atheroscerlois and CAD. But, LDL with a 100 to 160 mg concentration, is in constant circulation, in a smooth manner serving other physiological vascular functions.

The forcible evidence that LDL can pierce an Intact endothelium is so huge no one can have the courage to dispute it. But, it doesn’t happen in the majority is the mysterious truth.

Electron microscopic picture of 20nm sized LDL molecules in circulation. They are not as frightening molecules as they are portrayed

What factors induce LDL to enter the endothelial gap junctions.?

Some facts

The diameter of LDL particles is about 20–30 nm which is much larger than that of gap-junctions (3–6 nm) between adjacent cells in continuous endothelium (Iuliano, Micheletta, & Violi, 2001). Hence, the only way for LDLs to cross the endothelium is through a process called caveolae-mediated transcytosis.

Contrary to the shout-out, LDL is not a true villain in all patients with CAD. It is something else, we aren’t aware of that keeps the LDL either passive or promotes its penetration.

There are at least five important factors.

1. Baseline Endothelial Integrity & vascular aging

2. Accelerated caveolae formation,

3,The shear stress of flowing BP .

4 .The associated diabetic basement membrane dysfunction.

5. Finally, the aggressiveness of native LDL molecule (Absolute levels of LDL are less important than we think . Please note, the much-researched South Asian metabolic syndrome has near normal LDL )

What we fail to acknowledge is the fact that our understanding of endothelial lipid interaction is based on poor-quality data . Meanwhile, the concept of endothelial-friendly LDL can’t be eliminated totally.

Final message

How many molecules of LDL enter endothelial breakpoints?

I am sure, no one can answer this question. In fact, this question need not be answered. Still, the PCSK blockers, the Inclisirons are the new armed weapons in anti LDL industry waiting hungrily to Invade the vasculature. What if these agents swallow good LDLs ?

Let us first clarify, the true invading potential of LDL before falling for these costly semi-annual subscription-based drugs. Meanwhile, HDL dysfunction with its Apo A2 interaction defects may be a more concerning issue than LDL-mediated injury is coming up.

Reference

1. Francesca Luchetti, Rita Crinelli, Maria Gemma Nasoni, Serena Benedetti, Francesco Palma, AlessaLDL receptors, caveolae and cholesterol in endothelial dysfunction: oxLDLs accomplices or victims ? British Journal of pharmacology.

https://doi.org/10.1111/bph.15272

Leriche syndrome (1948, Annals of Surgery, College de Paris, France) is a famous eponym in Aortic vascular emergency, where a saddle-shaped thrombus folds across the Aortic bi-furcation resulting in bilateral lower limb vascular insufficiency.

Though such vascular emergencies can occur in any bifurcation point in a vascular tree, it is not often thought about in acute coronary syndrome.

Large thrombus burden in LAD or LCX is so commonly visualized, while in a stump left main, we often fail to recognize the fact, that it is almost the same as “saddle embolus” sitting across both LAD & LCX bifurcation.

Most such patients do not reach the hospital. If the thrombus migrates to one of the branches, it might evolve either as LAD STEMI, LCX STEMI, or a combination of both. We have seen a few lucky Left main STEMIs in the cath lab, with some spontaneous canalization.

Final message

De-novo Coronary Leriche syndrome is a real entity. For many of us this may appear, just an acute coronary curiosity, since most of the time it results in silent sudden deaths and escapes from our vision. However, primary PCI Interventionalists need to be aware of this concept, as meddling in this critical arena with high thrombus load can rapidly evolve into an acquired Leriche syndrome, for which the operator becomes squarely responsible.

Reference

1.Leriche R, Morel A. The Syndrome of Thrombotic Obliteration of the Aortic Bifurcation. Ann Surg. 1948 Feb;127(2):193-206. doi: 10.1097/00000658-194802000-00001. PMID: 17859070; PMCID: PMC1513778.

Link 2

1. Wrap around LAD true Global MI

2. RCA-dependent LAD circulation through collaterals

3. True bifurcation STEMI with static thrombus  (Carinal trapping of thrombus  ,Coronary Lerish sydrome )

4. Embolic  STEMI with showers of emboli  into both LCX and LAD

Simultaneous or sequential Anterior and Inferior STEMI

5. Mid or Proximal LAD lesion with proximal thrombus build-up

Further possibilities 

 Mimickers: Distal LAD lesions -Inferior ST elevation due to sparing of diagonal

 Wrong diagnosis -ERS pattern, pericarditis etc.

We have more than solid evidence, that rate control is good enough or even better than rhythm control in the management of AF , for more than two decades. Studies that showed either equipoise or rate control was marginally superior in certain clinical parameters are.

1.AFFIRM (2002)

2.RACE

3.STAF(2003)

4.HOT-CAFE (2004)

Now, in 2020s with modalities like ablation, the choice is being pushed toward Pro-rhythm control. (Of course with evidence).Some of these studies are,

1.EAST-AFNET (2020)

2.CASTLE AF(2018)

3.RAFT AF (Again equivocal)

With emerging new technologies, scientists are trying whether more safer methods like cryoablation or pulse-filed ablation would beat the rate control with drugs. Still, rhythm control strategy is finding it tough to win over the apparently less scientific rate control strategy. (Why? The reason is discussed elsewhere )

“How can rhythm control be inferior or non-superior? Something is wrong. We can’t leave it like that. Let’s do a meta-analysis”

Even meta-analysis couldn’t help out rhythm control strategy.(Caldeira, Daniel et al. “Rate versus rhythm control in atrial fibrillation and clinical outcomes: updated systematic review and meta-analysis of randomized controlled trials.” Archives of cardiovascular diseases 105 4 (2012): 226-38 .)

Now, what shall we do? , Let us do another meta-analysis. A fresh one is released just a few days ago in 2024 . This mega meta-analysis with almost similar data, clearly vouchs for the superiority of early rhythm control with some form of ablation. It is gratifying that, with this study, we could sustain some confusion, in the management of this most common cardiac arrhythmia.

When will this fight for Rate vs Rhythm control in AF end?

Answer: It will not stop as long as an entity AF exists. Research, as the name implies, we need to search again, & again for truth. However, In the case of AF, I think, a different game is being played in the EP arena. It looks like, we are fighting with an established truth, not fighting for the truth.

Reference

1.Stefanos Zafeiropoulos, Ioannis Doundoulakis, Alexandra Bekiaridou et al Rhythm vs Rate Control Strategy for Atrial Fibrillation: A Meta-Analysis of Randomized Controlled Trials J Am Coll Cardiol EP. May 08, 2024. Epublished DOI: 10.1016/j.jacep.2024.03.006